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Endothelial Cells Stimulate Self-Renewal and Expand Neurogenesis of Neural Stem Cells
TLDR
It is shown that endothelial cells but not vascular smooth muscle cells release soluble factors that stimulate the self-renewal of neural stem cells, inhibit their differentiation, and enhance their neuron production. Expand
Cellular levels of p120 catenin function as a set point for cadherin expression levels in microvascular endothelial cells
TLDR
Results demonstrate that cellular levels of p120ctn function as a set point mechanism that regulates cadherin expression levels, and that a major function of p 120ctn is to control cadher in internalization and degradation. Expand
p120-catenin binding masks an endocytic signal conserved in classical cadherins
p120 regulates adhesive junction dynamics through binding to a dual-function motif in classical cadherins that alternately serves as a p120-binding interface and an endocytic signal.
p120-Catenin regulates clathrin-dependent endocytosis of VE-cadherin.
TLDR
A novel mechanism by which a cytoplasmic binding partner for a transmembrane receptor can serve as a selective plasma membrane retention signal, thereby modulating the availability of the protein for endo-lysosomal processing is suggested. Expand
VE-cadherin: adhesion at arm's length.
TLDR
A series of new studies place p120(ctn) at the hub of a cadherin-catenin regulatory mechanism that controls cadher in plasma membrane levels in cells of both epithelial and endothelial origin. Expand
Electrical Impedance of Cultured Endothelium Under Fluid Flow
TLDR
It is demonstrated that the impedance of endothelial monolayers changes dynamically with flow indicating morphological and/or functional changes in the cell layer. Expand
Src-induced Tyrosine Phosphorylation of VE-cadherin Is Not Sufficient to Decrease Barrier Function of Endothelial Monolayers*♦
TLDR
It is suggested that signaling leading to changes in vascular permeability in response to inflammatory mediators or growth factors may require VE-cadherin tyrosine phosphorylation concurrently with other signaling pathways to promote loss of barrier function. Expand
Activated Ras induces a proangiogenic phenotype in primary endothelial cells
TLDR
The data suggest that the acquisition of activating Ras mutations can lead to a proangiogenic conversion in the phenotype of primary endothelial cells and raise the possibility that chronic Ras activation in endothelium cells may be sufficient to promote angiogenesis and the development of vascular anomalies. Expand
Creating perfused functional vascular channels using 3D bio-printing technology.
TLDR
A methodology using 3D bio-printing technology to create a functional in vitro vascular channel with perfused open lumen using only cells and biological matrices to investigate fundamental mechanisms of vascular remodeling with extracellular matrix and maturation process under 3D flow condition. Expand
RhoA and Rho-kinase dependent and independent signals mediate TGF-beta-induced pulmonary endothelial cytoskeletal reorganization and permeability.
TLDR
The data suggest: 1) the RhoA/Rho-kinase pathway is an important component of TGF-beta-induced effects on endothelial MLC phosphorylation, cytoskeletal reorganization, and barrier integrity; and 2) additional signaling mechanisms independent of the RHoA/ Rho- Kinase signaling cascade contribute to TGF -beta- induced changes in cytOSkeletal organization and permeability. Expand
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